Asthma exacerbation related to viral infections: An up to date summary

Adeli, Mehdi; El-Shareif, Tamara; Hendaus, Mohamed A.

doi:10.4103/jfmpc.jfmpc_86_19

Cited by 34 publications

(48 citation statements)

References 76 publications

(125 reference statements)

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“…These observations reinforce the idea that asthma exacerbations can be promoted by viral respiratory infections [3]. Asthmatic exacerbations consist of episodes characterized by an increase in respiratory symptoms (dyspnoea, cough, wheezing, chest tightness) and worsening of lung function requiring changes of therapy, the intake of oral corticosteroids (OCS), emergency treatment and hospitalization in the most severe cases [2,3]. In terms of pulmonary function tests, asthma exacerbation is defined as a > 20% reduction in FEV1 (Forced Expiratory Volume in 1 second) from baseline or a > 30% reduction in peak expiratory flow (PEF) for 2 consecutive days.…”

Section: Introductionsupporting

confidence: 85%

“…Viral respiratory infections are recognized risk factors for the loss of control of allergic asthma and the induction of exacerbations, both in adults and children [1][2][3]. Almost 80% of asthma exacerbations were associated with viral infections [1][2][3]. Severe asthma is more susceptible to virus-induced asthma exacerbations, especially in the presence of high IgE levels [4,5].…”

Section: Introductionmentioning

confidence: 99%

“…HRV viruses are the most common causative agents found in the 5 days preceding the development of exacerbations [3]. Several studies showed seasonal variations in hospital admissions for asthma related to viral upper respiratory tract infections, with higher rates of asthma exacerbations in autumn (28.8%) and spring (19.6%) [3]. The frequency of asthma exacerbations in autumn, winter and spring was 1.5-2 times higher than the one observed in summer in both adults and adolescents, if not adequately treated [7].…”

Section: Introductionmentioning

confidence: 99%

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Immunological Aspects Related to Viral Infections in Severe Asthma and the Role of Omalizumab

Menzella¹,

Ghidoni²,

Galeone³

et al. 2021

Preprint

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Viral respiratory infections are recognized risk factors for the loss of control of allergic asthma and the induction of exacerbations, both in adults and children. Severe asthma is more susceptible to virus-induced asthma exacerbations, especially in the presence of high IgE levels. In the course of immune responses to viruses, an initial activation of innate immunity typically occurs and the production of type I and III interferons is essential in the control of viral spread. However, the Th2 inflammatory environment still appears to be protective against viral infections in general and in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections as well. As for now, literature data, although very limited and preliminary, show that severe asthma patients treated with biologics don’t have an increased risk of SARS-CoV-2 infection or progression to severe forms compared to the non-asthmatic population. Omalizumab, an anti-IgE monoclonal antibody, exerts a profound cellular effect, which is able to stabilize the effector cells becoming much more efficient from the point of view of innate immunity in contrasting respiratory viral infections. In addition to the antiviral effect, clinical efficacy and safety of this biological allows a great improvement in the management of asthma.

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Section: Introductionsupporting

confidence: 85%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Immunological Aspects Related to Viral Infections in Severe Asthma and the Role of Omalizumab

Menzella¹,

Ghidoni²,

Galeone³

et al. 2021

Preprint

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“…These agents elicit an immune response leading to infiltration of activated immune cells that further release inflammatory mediators that cause acute symptoms such as increased mucus production, cough, wheeze and shortness of breath. Among these agents, viral infection is one of the major drivers of asthma exacerbations accounting for up to 80-90% and 45-80% of exacerbations in children and adults respectively (Grissell et al, 2005;Xepapadaki and Papadopoulos, 2010;Jartti and Gern, 2017;Adeli et al, 2019). Viral involvement in COPD exacerbation is also equally high, having been detected in 30-80% of acute COPD exacerbations (Kherad et al, 2010;Jafarinejad et al, 2017;Stolz et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Respiratory Viral Infections in Exacerbation of Chronic Airway Inflammatory Diseases: Novel Mechanisms and Insights From the Upper Airway Epithelium

Tan

Lim

Liu

et al. 2020

Front. Cell Dev. Biol.

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Respiratory virus infection is one of the major sources of exacerbation of chronic airway inflammatory diseases. These exacerbations are associated with high morbidity and even mortality worldwide. The current understanding on viral-induced exacerbations is that viral infection increases airway inflammation which aggravates disease symptoms. Recent advances in in vitro air-liquid interface 3D cultures, organoid cultures and the use of novel human and animal challenge models have evoked new understandings as to the mechanisms of viral exacerbations. In this review, we will focus on recent novel findings that elucidate how respiratory viral infections alter the epithelial barrier in the airways, the upper airway microbial environment, epigenetic modifications including miRNA modulation, and other changes in immune responses throughout the upper and lower airways. First, we reviewed the prevalence of different respiratory viral infections in causing exacerbations in chronic airway inflammatory diseases. Subsequently we also summarized how recent models have expanded our appreciation of the mechanisms of viral-induced exacerbations. Further we highlighted the importance of the virome within the airway microbiome environment and its impact on subsequent bacterial infection. This review consolidates the understanding of viral induced exacerbation in chronic airway inflammatory diseases and indicates pathways that may be targeted for more effective management of chronic inflammatory diseases.

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“…Exacerbations are a major cause of disease morbidity and mortality in asthma, and they have been associated with increased loss of lung function in asthma [1]. Up to 70% of exacerbations in adult asthma are associated with respiratory viral infections [2], with rhinovirus (RV) being the most common cause of asthma exacerbations [3]. Viruses can trigger innate immune responses via the activation of Toll-like receptors (TLRs), such as TLR3 and TLR7/8, or the RIG-I-like helicases, melanoma differentiation-associated protein 5 (MDA5) and retinoic acid-inducible gene 1 (RIG-I).…”

Section: Introductionmentioning

confidence: 99%

TLR3/TAK1 signalling regulates rhinovirus-induced interleukin-33 in bronchial smooth muscle cells

et al. 2020

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BackgroundAsthma exacerbations are commonly associated with rhinovirus (RV) infection. Interleukin-33 (IL-33) plays an important role during exacerbation by enhancing Type 2 inflammation. Recently we showed that RV infects bronchial smooth muscle cells (BSMCs) triggering production of interferons and IL-33. Here we compared levels of RV-induced IL-33 in BSMCs from healthy and asthmatic subjects, and explored the involvement of pattern-recognition receptors (PRRs) and downstream signalling pathways in IL-33 expression.MethodBSMCs from healthy and severe and non-severe asthmatic patients were infected with RV1B or stimulated with the PRR agonists poly(I:C) (Toll-like receptor 3 (TLR3)), imiquimod (TLR7) and poly(I:C)/LyoVec (retinoic acid-inducible gene 1 (RIG-I)/melanoma differentiation-associated protein 5 (MDA5)). Knockdown of TLR3, RIG-I and MDA5 was performed, and inhibitors targeting TBK1, nuclear factor-κB (NF-κB) and transforming growth factor (TGF)-β-activated kinase 1 (TAK1) were used. Gene and protein expression were assessed.ResultsRV triggered IL-33 gene and protein expression in BSMCs. BSMCs from patients with non-severe asthma showed higher baseline and RV-induced IL-33 gene expression compared to cells from patients with severe asthma and healthy controls. Furthermore, RV-induced IL-33 expression in BSMCs from healthy and asthmatic individuals was attenuated by knockdown of TLR3. Inhibition of TAK1, but not NF-κB or TBK1, limited RV-induced IL-33. The cytokine secretion profile showed higher production of IL-33 in BSMCs from patients with non-severe asthma compared to healthy controls upon RV infection. In addition, BSMCs from patients with non-severe asthma had higher levels of RV-induced IL-8, TNF-α, IL-1β, IL-17A, IL-5 and IL-13.ConclusionRV infection caused higher levels of IL-33 and increased pro-inflammatory and Type 2 cytokine release in BSMCs from patients with non-severe asthma. RV-induced IL-33 expression was mainly regulated by TLR3 and downstream via TAK1. These signalling molecules represent potential therapeutic targets for treating asthma exacerbations.

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Asthma exacerbation related to viral infections: An up to date summary

Cited by 34 publications

References 76 publications

Immunological Aspects Related to Viral Infections in Severe Asthma and the Role of Omalizumab

Immunological Aspects Related to Viral Infections in Severe Asthma and the Role of Omalizumab

Respiratory Viral Infections in Exacerbation of Chronic Airway Inflammatory Diseases: Novel Mechanisms and Insights From the Upper Airway Epithelium

TLR3/TAK1 signalling regulates rhinovirus-induced interleukin-33 in bronchial smooth muscle cells

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